All participants or their family members were informed about the potential publication of their identities and images, and all of them completed consent forms. All procedures and protocols were approved by the ethics committee of Beijing Anzhen Hospital, Capital Medical University, and the experiments were conducted in accordance with the Declaration of Helsinki (1975 and subsequent revisions).
Between January 2016 and December 2017, 480 patients (400 men and 80 women) with acute STEMI who underwent PPCI treatment in Beijing Anzhen Hospital were enrolled in this retrospective study. Clinical and angiographic follow-up was performed in all patients for 12 months. The inclusion criteria were as follows. (1) Acute myocardial infarction lasting for <12 h and only one NCL found in the setting of STEMI. Acute myocardial infarction was defined as follows: evidence of ischemic chest pain lasting for >30 min, and new ST segment elevation of ≥2 mm in two or more contiguous electrocardiographic leads; a de novo lesion; single vessel treatment in a native vessel ≥2.5 mm in diameter and occluded, thrombus containing; thrombolysis in myocardial infarction (TIMI) flow grade of 0 to 2 in the culprit artery, and the grade of stenosis of NCLs was <70%. (2) There was no contraindication for anticoagulation and antiplatelet therapy.
The main exclusion criteria included the following: previous percutaneous coronary intervention (PCI) in an infarction-related artery (IRA) (n = 7), Killip class ≥3 (n = 8), left or right bundle branch block (n = 10), IRA with excessive proximal tortuosity or severe calcification (n = 13), left ventricular ejection fraction <35% (n = 14), lack of clinical and angiographic follow-up (n = 25), in-hospital death after PPCI (n = 10), myocardial infarction within 2 w of PPCI to exclude potential subacute stent thrombosis of the intervened arterial segment (n = 8), and repeated PCI of culprit coronary lesions for restenosis or progression (n = 41).
Coronary angiography was performed using the Judkins method, and coronary artery lesion classification was based on the American College of Cardiology/American Heart Association guidelines[3] .Thrombus aspiration catheters (DIVER CE, Invatec, Brescia, Italy) were used for thrombotic burden lesions. Stents were implanted using a routine method, and the procedure succeeded with residual stenosis <20%, TIMI flow grade of 3 and no acute complications (death, myocardial infarction, emergency coronary artery bypass grafting (CABG)), and no major adverse cardiac events (cardiac death, myocardial infarction, target vessel revascularization). Clinical and angiography follow-up was performed for 12 months.
The culprit coronary lesions were clearly identified through a combination of electrocardiography and coronary angiography. NCLs were defined as those with a diameter of stenosis <70%. All patients underwent PPCI for the culprit lesions.
Quantitative coronary angiography was performed during the first angiography. Follow-up angiography was performed by two independent investigators who were blinded to the results. We categorized the lesions in accordance with the American College of Cardiology/American Heart Association. Classification was performed on the basis of the morphological characteristics of lesions that cause significant stenosis of the coronary arteries.[3] These include two categories of simple lesions (A or B1 lesions) and complex lesions (B2 or C).
The collected data included demographic information, medical history, coronary artery disease risk factor status, detailed coronary angiographic information, biomarkers associated with coronary atherosclerosis at the time of baseline PCI, and coronary angiographic information at the time of angiographic follow-up.
All clinical, laboratory, and coronary angiographic data were evaluated by two independent investigators who were not involved in the angiographic procedures.
Definition of NCL progression [3]: 1. The stenosis degree of the NCL was ≥50% at the time of baseline PCI, and the degree of NCL progression was ≥10% at the time of angiographic follow-up. 2. The stenosis degree of the NCL was <50% at the time of baseline PCI, and the degree of NCL progression was ≥30% at the time of angiographic follow-up. 3. The degree of NCL progression ≥30%, while there were no NCLs at the time of baseline PCI. 4. NCL progression to total occlusion.
Hypertension was defined as systolic blood pressure >140 mmHg (1 mmHg = 0.133 kPa)/and/or diastolic blood pressure >90 mmHg, or patients were taking antihypertensive drugs, in accordance with the 2010 Chinese Hypertension Prevention Guide revised edition[4] .
Diabetes was defined as the typical symptoms of diabetes (drinking more, polyphagia, polyuria, weight loss) and fasting plasma glucose >7.0/L or blood sugar >1 (with a tendency towards 1.1) 2 h after an oral glucose tolerance test, in accordance with the China Guideline for the Prevention of Type 2 Diabetes (2017 Edition)[5] .
SPSS20.0 software was used for all statistical analyses. Count data are expressed as cases and percentages, and the χ2 test was used for analysis. Numerical data are expressed as mean ± SD and were compared using the Student’s t test. Non-normally distributed numerical data are expressed as the median and 25th–75th interquartile range and were compared using a rank-sum test. A partial correlation analysis was used to evaluate the correlations between fasting blood glucose (FBG), and progression of NCL. Binary logistic regression analysis was performed to examine independent risk factors for the progression of NCL. Receiver-operating characteristic (ROC) analysis and a calculation of sensitivity and specificity were performed to test the ability of FBG to predict the progression of NCL. A P value of less than 0.05 was considered statistically significant.
All patients were divided into the control group (without NCL progression) and the progression group (with NCL progression) in accordance with the definition of NCL progression.